General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 611: What is the benign neoplasm of brown fat noted in the oral/pharyngeal region?

A. Lipoma
B. Hibernoma (Correct Answer)
C. Teratoma
D. Brown tumor

Explanation: **Explanation:** **Hibernoma** is a rare, benign soft tissue tumor composed of **brown fat**. The name is derived from its resemblance to the brown adipose tissue found in hibernating animals. In humans, brown fat is primarily found in neonates for non-shivering thermogenesis, but remnants persist in adults in the neck, axilla, mediastinum, and retroperitoneum. While rare, hibernomas can occur in the oral cavity and pharyngeal regions. **Histopathology Key:** They are characterized by large, multivacuolated cells with granular, eosinophilic cytoplasm (rich in mitochondria) and a small, central nucleus. [1] **Analysis of Incorrect Options:** * **A. Lipoma:** This is the most common benign mesenchymal tumor, but it is composed of **mature white adipose tissue**, not brown fat. [1] * **C. Teratoma:** These are germ cell tumors containing tissues derived from more than one germ layer (ectoderm, mesoderm, endoderm). [2], [3] While they can occur in the head and neck (e.g., epignathus), they are not specific to brown fat. * **D. Brown Tumor:** Despite the name, this is **not a neoplasm**. It is a non-neoplastic lesion associated with **Hyperparathyroidism**. It consists of giant cell-rich lesions and gets its "brown" color from hemosiderin deposition, not brown fat. **NEET-PG High-Yield Pearls:** * **Brown Fat vs. White Fat:** Brown fat contains multiple lipid droplets (multilocular) and high mitochondrial density (expressing **UCP-1/thermogenin**), whereas white fat has a single large droplet (unilocular). * **Imaging:** On PET scans, Hibernomas show **intense FDG uptake** due to high metabolic activity, which can sometimes be mistaken for malignancy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1222. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1033-1034. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482.

Question 612: What is the typical number of chromosomes in an individual with Klinefelter syndrome?

A. 47 (Correct Answer)
B. 46
C. 45
D. 44

Explanation: **Explanation:** **Klinefelter Syndrome** is the most common sex chromosome disorder affecting males, occurring in approximately 1 in 600 live births [1]. The correct answer is **47** because the syndrome is characterized by **aneuploidy**, specifically the presence of at least one extra X chromosome [1]. * **Why 47 is correct:** The classic karyotype for Klinefelter syndrome is **47,XXY** [1]. This occurs due to **meiotic non-disjunction** of sex chromosomes during gametogenesis (more commonly maternal). The presence of the Y chromosome ensures a male phenotype, while the extra X chromosome leads to testicular dysgenesis. * **Why 46 is incorrect:** This represents the normal human diploid number (46,XY or 46,XX). * **Why 45 is incorrect:** This is seen in **Turner Syndrome (45,X)**, which is the most common monosomy in humans. * **Why 44 is incorrect:** An autosome count of 44 is normal, but a total chromosome count of 44 is generally incompatible with life. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Features:** Tall stature, long legs, small firm testes (testicular atrophy), gynecomastia, and female-type hair distribution. * **Biochemical Profile:** Increased FSH and LH (due to loss of feedback inhibition) and **decreased Testosterone**. * **Histology:** Hyalinization and fibrosis of seminiferous tubules with **Leydig cell hyperplasia** (apparent). * **Key Association:** Increased risk of **Male Breast Cancer** (20x higher than normal), extragonadal germ cell tumors, and autoimmune diseases like SLE. * **Barr Body:** Unlike normal males, Klinefelter patients are **Barr body positive** (calculated as $n-1$, where $n$ is the number of X chromosomes). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 92-93.

Question 613: Which of the following is false regarding cystic fibrosis?

A. Associated with the CFTR gene
B. Autosomal recessive inheritance
C. Associated with chromosome 7p (Correct Answer)
D. Recurrent respiratory tract infection

Explanation: **Explanation:** Cystic Fibrosis (CF) is a multisystemic disorder caused by mutations in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene [1]. **Why Option C is the Correct (False) Statement:** The CFTR gene is located on the **long arm (q)** of **Chromosome 7**, specifically at position **7q31.2**. Option C incorrectly states it is on the short arm (p). In medical genetics, distinguishing between the 'p' (petite/short) and 'q' (long) arms is a frequent high-yield distinction in competitive exams. **Analysis of Other Options:** * **Option A:** The disease is caused by a defect in the **CFTR gene**, which codes for a chloride channel [1]. The most common mutation is **ΔF508** (deletion of phenylalanine at position 508) [2]. * **Option B:** CF follows an **Autosomal Recessive** inheritance pattern [5]. It is the most common lethal genetic disease in Caucasian populations [5]. * **Option D:** Defective chloride transport leads to abnormally thick, viscid mucus [1]. This causes impaired mucociliary clearance, leading to **recurrent respiratory infections**, bronchiectasis, and colonization by pathogens like *Pseudomonas aeruginosa* and *Staphylococcus aureus* [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Sweat Chloride Test (Gold Standard) showing chloride levels **>60 mmol/L**. * **Gastrointestinal:** Meconium ileus (newborns), pancreatic insufficiency (leading to malabsorption and Steatorrhea) [3], and biliary cirrhosis. * **Reproductive:** Infertility in males due to **Congenital Bilateral Absence of Vas Deferens (CBAVD)** [3]. * **Nasal Polyps:** CF is a common cause of nasal polyposis in children. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Lumen Of Sweat Duct, pp. 475-476. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 476. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 476-477. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 478. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 120-122.

Question 614: A permanent tooth with a local hypoplastic deformity in a crown is called?

A. Turner's tooth (Correct Answer)
B. Taurodontism
C. Enameloma
D. Ghost teeth

Explanation: ### Explanation **Turner’s Tooth (Turner’s Hypoplasia)** The correct answer is **Turner’s tooth**. This condition refers to a permanent tooth that exhibits a localized enamel hypoplastic deformity. It most commonly occurs due to an **extension of periapical infection** from the overlying deciduous tooth or **local mechanical trauma** during the development of the permanent tooth bud. The inflammatory process or trauma disrupts the ameloblasts (enamel-forming cells), leading to defects ranging from white/brown discoloration to severe pitting and coronal deformity. It most frequently affects permanent premolars. **Analysis of Incorrect Options:** * **Taurodontism:** This is a morphologic variation where the tooth body is elongated and the roots are shortened, leading to an apical displacement of the furcation ("bull-like" teeth). It is a shape anomaly, not a localized enamel hypoplasia. * **Enameloma (Enamel Pearl):** This is a small, focal mass of ectopic enamel found typically on the root surface, especially near the bifurcation of molar teeth. * **Ghost Teeth (Regional Odontodysplasia):** This is a rare developmental anomaly affecting all dental tissues (enamel, dentin, and pulp) in a specific quadrant. On X-ray, these teeth appear thin and shell-like with very little mineralization, giving them a "ghostly" appearance. **High-Yield NEET-PG Pearls:** * **Most common site:** Permanent maxillary incisors (due to trauma) or permanent premolars (due to periapical infection of deciduous molars). * **Amelogenesis Imperfecta:** Unlike Turner’s tooth (which is localized/acquired), Amelogenesis Imperfecta is a genetic condition affecting the enamel of *all* teeth. * **Syphilitic Hypoplasia:** Congenital syphilis causes specific enamel defects known as **Hutchinson’s incisors** (notched) and **Mulberry molars** (globular occlusal surfaces).

Question 615: Which of the following is NOT a mononuclear-macrophage?

A. Histiocytes
B. Microglia
C. Kupffer cells
D. B-cells (Correct Answer)

Explanation: The **Mononuclear Phagocyte System (MPS)**, formerly known as the Reticuloendothelial System, consists of a lineage of cells derived from hematopoietic stem cells in the bone marrow. These cells differentiate into blood monocytes and eventually migrate into various tissues to become specialized, long-lived tissue macrophages. ### Why B-cells are the Correct Answer: **B-cells** are lymphocytes, not macrophages [1]. While both B-cells and macrophages are "Professional Antigen Presenting Cells" (APCs) and share a common lymphoid-myeloid progenitor, B-cells belong to the **lymphoid lineage** [2]. Their primary function is humoral immunity (antibody production) rather than phagocytosis [1]. Unlike the other options, B-cells do not arise from the monocyte-macrophage cell line. ### Explanation of Incorrect Options: * **Histiocytes:** These are the resident macrophages of **connective tissue**. They are the classic example of tissue-fixed mononuclear phagocytes. * **Microglia:** These are the specialized macrophages of the **Central Nervous System (CNS)**. They are unique because they migrate to the brain during the early embryonic period. * **Kupffer cells:** These are specialized macrophages located in the **sinusoids of the liver**, responsible for clearing pathogens and aged red blood cells from the portal circulation. ### NEET-PG High-Yield Pearls: * **Other MPS members to remember:** Alveolar macrophages (Lung/Dust cells), Osteoclasts (Bone), Langerhans cells (Skin), and Mesangial cells (Kidney). * **Origin:** Most tissue macrophages are derived from embryonic yolk sac or fetal liver progenitors and maintain themselves by local proliferation, though they can be supplemented by blood monocytes during inflammation. * **Marker:** **CD68** is the most common immunohistochemical marker used to identify cells of the macrophage lineage. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 579-580. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 551-552.

Question 616: Edward syndrome is characterized by which of the following chromosomal abnormalities?

A. Trisomy 13
B. Trisomy 18 (Correct Answer)
C. Trisomy 21
D. Trisomy 20

Explanation: **Explanation:** **Edward Syndrome** is a chromosomal disorder caused by **Trisomy 18** (the presence of an extra copy of chromosome 18) [1]. It is the second most common autosomal trisomy among live births, following Down syndrome [1]. The condition is characterized by severe intellectual disability and multi-system congenital anomalies, with a very low survival rate beyond the first year of life [2]. **Analysis of Options:** * **Option B (Trisomy 18):** This is the correct chromosomal abnormality. The extra genetic material interferes with normal development, leading to classic features such as **clenched fists with overlapping fingers**, rocker-bottom feet, and micrognathia [1]. * **Option A (Trisomy 13):** This refers to **Patau Syndrome** [1]. It is clinically distinguished by midline defects such as holoprosencephaly, cleft lip/palate, and polydactyly. * **Option C (Trisomy 21):** This refers to **Down Syndrome**, the most common autosomal trisomy [1]. It is characterized by flat facial profiles, Simian creases, and Brushfield spots [3]. * **Option D (Trisomy 20):** This is a rare chromosomal abnormality, often occurring as mosaicism, and is not associated with Edward syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (E for Edward):** **E**ighteen (18), **E**ars (low-set), **E**longated skull (prominent occiput), and **E**lection (clenched fists/overlapping fingers). * **Key Features:** Rocker-bottom feet (also seen in Patau), micrognathia, and congenital heart defects (VSD, PDA). * **Prenatal Screening:** Triple/Quadruple screen typically shows **decreased** levels of AFP, hCG, and unconjugated estriol (uE3). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-171.

Question 617: Cytosolic cytochrome C plays an important function in?

A. Apoptosis (Correct Answer)
B. Cell necrosis
C. Electron transport chain
D. Cell division

Explanation: **Explanation:** The correct answer is **Apoptosis (Option A)**. **Why Apoptosis is correct:** Cytochrome C is a key component of the **Intrinsic (Mitochondrial) Pathway** of apoptosis [1]. Under normal conditions, Cytochrome C is sequestered within the inner mitochondrial membrane. When a cell undergoes stress (e.g., DNA damage or growth factor withdrawal), the pro-apoptotic proteins **BAX and BAK** create pores in the mitochondrial membrane [2]. This allows Cytochrome C to leak into the **cytosol**. Once in the cytosol, Cytochrome C binds to **Apaf-1** (Apoptotic protease activating factor-1), forming a wheel-like hexamer called the **Apoptosome**. This complex activates **Caspase-9**, the initiator caspase of the intrinsic pathway, leading to programmed cell death [1]. **Why other options are incorrect:** * **Cell Necrosis (B):** Necrosis is an accidental, unregulated form of cell death characterized by membrane rupture and inflammation. It does not involve the specific cytochrome C-caspase signaling cascade. * **Electron Transport Chain (C):** While Cytochrome C is involved in the ETC, its function there occurs **inside the mitochondria** (intermembrane space). The question specifically asks about **cytosolic** Cytochrome C, which is a pathological state signaling apoptosis. * **Cell Division (D):** Cytochrome C has no direct regulatory role in the cell cycle or mitosis. **High-Yield Clinical Pearls for NEET-PG:** * **BCL-2 and BCL-XL:** These are anti-apoptotic proteins that prevent the release of Cytochrome C by stabilizing the mitochondrial membrane [2]. * **Executioner Caspases:** Both intrinsic and extrinsic pathways converge on Caspases **3 and 6**. * **Mnemonic:** "C" for **C**ytochrome **C** leads to **C**aspase activation. * **Biochemical Marker:** The presence of Cytochrome C in the cytosol is a definitive biochemical marker that the cell has committed to the intrinsic pathway of apoptosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-67. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 80-81.

Question 618: Which of the following is the hallmark of programmed cell death?

A. Apoptosis (Correct Answer)
B. Coagulation necrosis
C. Fibrinoid necrosis
D. Liquefaction necrosis

Explanation: **Explanation:** **Apoptosis** is the correct answer because it is the definition of **programmed cell death** [1]. It is a highly regulated, energy-dependent (ATP-requiring) pathway where a cell activates intrinsic enzymes to degrade its own DNA and proteins [2]. Unlike necrosis, apoptosis can be both physiological (e.g., embryogenesis, endometrial shedding) and pathological (e.g., DNA damage, viral infections) [1]. **Analysis of Incorrect Options:** * **Coagulation Necrosis:** This is the most common form of necrosis, typically seen in ischemic injury (infarcts) in all solid organs except the brain. It is characterized by the preservation of the structural outline of the cell for several days. * **Fibrinoid Necrosis:** This is a specialized form of necrosis usually seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa). It is characterized by the deposition of immune complexes and fibrin in arterial walls, appearing bright pink (eosinophilic) on H&E stain. * **Liquefaction Necrosis:** This occurs when enzymatic digestion of dead cells results in a liquid viscous mass. It is classically seen in focal bacterial/fungal infections (abscesses) and **hypoxic death of cells within the Central Nervous System (CNS).** **NEET-PG High-Yield Pearls:** * **Hallmark of Apoptosis:** Intact plasma membrane (no inflammation) and **chromatin condensation** (pyknosis) followed by fragmentation (karyorrhexis). * **Biochemical Marker:** Presence of **Phosphatidylserine** on the outer leaflet of the cell membrane (the "eat-me" signal). * **Key Enzyme:** **Caspases** (Cysteine-aspartic proteases) [2]. * **DNA Pattern:** Characterized by **Step-ladder pattern** on gel electrophoresis (due to internucleosomal cleavage), whereas necrosis shows a "smear" pattern. **Necroptosis:** Considered a hybrid form of cell death, it shares a genetic program similar to programmed cell death [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-64. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71.

Question 619: Natural killer (NK) cells attack which of the following types of cells?

A. Cells which express MHC class I
B. Cells which are unable to express MHC class I (Correct Answer)
C. MHC cells which express MHC class II
D. Cells which are unable to express MHC class I

Explanation: Natural Killer (NK) cells are a type of cytotoxic lymphocyte critical to the innate immune system. Their function is governed by the **"Missing Self" hypothesis**. [1] **Why the correct answer is right:** NK cells possess two types of surface receptors: **Inhibitory receptors** and **Activating receptors**. * Normal healthy cells express **MHC Class I** molecules, which bind to the inhibitory receptors (e.g., KIR - Killer-cell Immunoglobulin-like Receptors) on NK cells, sending an "off" signal that prevents cell lysis. [1] * Virally infected cells or tumor cells often downregulate or lose MHC Class I expression to evade CD8+ T-cells. When an NK cell encounters a cell **unable to express MHC Class I**, the inhibitory signal is lost. This allows the activating receptors to trigger the release of perforins and granzymes, leading to apoptosis of the target cell. [1] **Analysis of Incorrect Options:** * **Option A:** Cells expressing MHC Class I provide an inhibitory signal to NK cells, protecting them from attack. [1] * **Option C:** MHC Class II is primarily expressed on Professional Antigen Presenting Cells (APCs) like macrophages and B-cells for interaction with CD4+ T-cells, not for NK cell regulation. [2] * **Option D:** (Note: This is a duplicate of the correct answer in the provided options). **High-Yield Facts for NEET-PG:** * **Markers:** NK cells are identified by the presence of **CD56** and **CD16** (Fc\u03b3RIII) and the absence of CD3. * **ADCC:** CD16 allows NK cells to bind to IgG-coated cells, mediating Antibody-Dependent Cellular Cytotoxicity (ADCC). * **Cytokine Production:** NK cells are a major source of **IFN-\u03b3**, which activates macrophages. [1] * **Morphology:** They are described as **Large Granular Lymphocytes (LGLs)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 156-157.

Question 620: Psammoma bodies show which type of calcification?

A. Metastatic
B. Dystrophic (Correct Answer)
C. Secondary
D. Any of the above

Explanation: **Explanation:** **1. Why Dystrophic Calcification is Correct:** Psammoma bodies are classic examples of **dystrophic calcification**. This process occurs in **non-viable or dying tissues** despite normal serum calcium and phosphate levels. The mechanism involves the deposition of calcium salts in single necrotic cells, which act as a "nidus" for further mineralization [1]. As layers of calcium salts accumulate concentrically, they form the characteristic microscopic, laminated, grit-like structures known as Psammoma bodies (from the Greek *psammos*, meaning sand) [1]. **2. Why Other Options are Incorrect:** * **Metastatic Calcification:** This occurs in **normal (living) tissues** and is always associated with **hypercalcemia** (e.g., hyperparathyroidism, vitamin D toxicity) [1], [2]. It typically affects the lungs, kidneys, and gastric mucosa [2]. * **Secondary Calcification:** This is not a standard pathological classification for the initial formation of Psammoma bodies. * **Any of the above:** Incorrect, as the pathogenesis of Psammoma bodies is specifically linked to localized cell death and membrane damage, not systemic mineral imbalances. **3. High-Yield Clinical Pearls for NEET-PG:** To remember the tumors associated with Psammoma bodies, use the mnemonic **"PSaMMoma"**: * **P:** **P**apillary carcinoma of the thyroid * **S:** **S**erous cystadenocarcinoma of the ovary * **M:** **M**eningioma * **M:** **M**esothelioma **Key Distinction:** * **Dystrophic:** Normal serum calcium + Dead/Injured tissue. * **Metastatic:** High serum calcium + Normal tissue. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 134-135. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 76-77.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Acute and Chronic Inflammation

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Tissue Repair and Wound Healing

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Hemodynamic Disorders

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Genetic Disorders

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Environmental Pathology

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Nutritional Diseases

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Molecular Basis of Disease

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